Research

Our thematic aims to address if and how histone modifications could be part of a –short-term– flexible epigenetic silencing mechanism, potentially involved in cell fate decisions. In this purpose, we are focusing on the so called bivalent chromatin structures. These structures are unusual because their histone H3 is concomitantly marked by the “active” H3K4me and the “repressive” H3K27me3 modifications. Bivalent domains were initially detected at promoters of many genes in both human and mouse ES cells. In the proposed model, bivalent chromatin domains act to repress gene transcription through H3K27me3, while keeping genes "poised" for alternative fates for when a differentiation pathway is induced by specific developmental cues However, their precise role in development remains controversial because probing the function of bivalent domains in developing organisms remains a challenge.

To gain insight into this important issue we analyse bivalency in two well defined frames, accounting for both normal and pathological contexts, namely in the genomic imprinting developmental process and in glioma tumors.